Coupling of metabolism and cardiovascular responses.

Abstract

We read with interest the paper by Fugmann et al. [1], in a previous issue of Clinical Science, showing the close link between metabolic changes, mimicking those of the postprandial state, and haemodynamic responses. We enjoyed, also, and wholeheartedly agree with, the accompanying Comment by Steinberg [2], arguing that these inter-related responses represent normal physiology. We have been studying for some time the response of ATBF (adipose tissue blood flow) to nutrient ingestion and infusion. In our studies and those of others, ATBF is much more responsive to nutrients than is skeletal muscle blood flow [3,4]; ATBF may increase 2.5-fold in response to glucose ingestion in a healthy subject [5]. Steinberg [2] therefore probably underestimates the importance of adipose tissue in the responses observed by Fugmann et al. [1] when interpreting these mostly in terms of skeletal muscle haemodynamics (the calf, after all, comprises more than muscle). We note the observation by Fugmann et al. [1] that normoglycaemic hyperinsulinaemia most closely mimics the postprandial state and their conclusion that ‘insulin is a major mediator of the haemodynamic changes seen following a mixed meal’. We have studied mediators of the ATBF response to nutrient ingestion. The timecourse of ATBF is closely parallel with that of plasma insulin [6], but insulin itself does not seem to be the local mediator [7]. In fact, the postprandial ATBF response is largely blocked by propranolol [8,9], implying insulindriven sympathetic activity as the key mediator. Similar to the observations on the whole calf by Fugmann et al. [1], ATBF is stimulated more by the insulin response following oral glucose than by equivalent elevation of glycaemic and insulinaemia produced by infusion [7], implying some role for gut-derived signals. Of further interest, we believe, is the situation when this close co-ordination between metabolism and haemodynamics breaks down. ATBF responsiveness to nutrients is blunted in obesity [10–12], and this impairment is closely related to insulin resistance measured in terms